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Respected sir, today I m going to talk about the prognosis n treatment aspect of ntsich.Intracerebral hemorrhage (ICH) is the second most common cause of stroke, after ischemic stroke in frequency [1,2]. There are many underlying pathological conditions associated with ICH; hypertension, amyloid angiopathy, ruptured saccular aneurysm, and vascular malformation account for the majority of cases.Hypertensive vasculopathy is the most common etiology of spontaneous ICH. Cerebral amyloid angiopathy is the most common cause of nontraumatic lobar ICH in the elderly, while vascular malformations are the most common cause of ICH in children [4]. Additional causes of nontraumatic ICH include:Hemorrhagic infarction (including venous sinus thrombosis).Septic embolism, mycotic aneurysm.Brain tumor.Bleeding disorders, anticoagulants, thrombolytic therapy.Central nervous system (CNS) infection (eg, herpes simplex encephalitis).Moyamoya.Vasculitis.Drugs (cocaine, amphetamines) [5]. Phenylpropanolamine in appetite suppressants, and possibly cold remedies, may be an independent risk factor for intracranial hemorrhage (including intracerebral hemorrhage and subarachnoid hemorrhage) in women [6,7].

BUT The prognosis after ICH depends upon the location of hemorrhage (supra versus infratentorial location), size of the hematoma, level of consciousness, patient age, and overall medical health and condition [3,4,6,9,11,12]. In addition, preceding oral anticoagulation therapy, and possibly antiplatelet therapy, appears to be associated with worse outcomes after ICH [9,13]. .it also depends on the underlying cause of the hemorrhage.

One study found that hemorrhage from a cerebral arteriovenous malformation were associated with a lower case-fatality rate, despite a similar hemorrhage volume and a higher admission Glasgow coma scale compared with spontaneous ICH [14]. Mortality was also reported to be low (1 of 22) in a cohort of children with ICH in whom vascular malformations was the identified etiology in 91 percent [15].

The 30-day mortality from ICH ranges from 35 to 52 percent [1-8]; one-half of these deaths occur within the first two days . Long-term survival after primary ICH also appears to be decreased compared with controls from the general population matched for age and sex.

The ICH volume on initial head CT scan and level of consciousness on admission may be particularly important prognostic indicators In a study of 188 patients with ICH that analyzed predictors of 30-day mortality [3]; the following observations were made:An ICH volume of 60 cm3 or greater on initial CT and a Glasgow coma scale score of eight or less predicted a 30-day mortality of 91 percent.An ICH volume less than 30 cm3 and a Glasgow coma scale score of nine or more predicted a 30-day mortality of 19 percent

Hematoma growth is also an independent predictor of mortality and poor outcome. Hemorrhage enlargement — Serial CT scans in patients with hypertensive hemorrhage have shown that the hemorrhage enlarges in the first six hours after presentation in a subset of patients [37,38]. In a prospective series of 103 patients with ICH, significant hematoma growth (a &gt;33 percent volume increase) occurred in 38 percent of patients over the first 24 hours [38].Pathologic studies prior to CT scanning found that bleeding points occurred in the rim of the hemorrhage and postulated that this new recruitment of bleeding sites would lead to enlargement of the clot. As the clot expands, surrounding vessels are stretched, causing new sites of vessel rupture. Although the precise mechanism of hemorrhage enlargement is not yet defined and may be heterogeneous, blood brain barrier breakdown and dysregulation of hemostasis via inflammatory cascade activation and MMP overexpression, as discussed above, is probably one important pathway. Elevated plasma concentrations of c-Fn and the inflammatory mediator interleukin-6 (IL-6) in the early acute phase of ICH have been associated with ICH enlargement [39]. However, the clinical utility of MMP, c-Fn, or IL-6 blood levels in early ICH is not yet clear.

Data from a number of studies suggest that extension of blood into the ventricles is an independent predictor of poor outcome in patients with spontaneous ICH [20-24].

Early neurologic deterioration within 48 hours after ICH onset is not infrequent and is associated with a poor prognosis. Potential mechanisms include hemorrhage enlargement, development of hydrocephalus, and perilesional edema [25]. The inflammatory response to the hemorrhage may also play a role.

Preceding antithrombotic use — In the setting of an acute ICH, patients with preceding use of anticoagulants or antiplatelet agents might be expected to have larger initial hematoma volumes or greater hemorrhage enlargement leading to worse outcomes.Oral anticoagulants — Patients on oral anticoagulant therapy have a mortality rate of 52 to 73 percent after ICH [13,30-32]. Furthermore, ICH related to oral anticoagulant therapy is associated with a worse outcome than spontaneous ICH, as illustrated by the following reports:

— Patients on oral anticoagulant therapy have a mortality rate of 52 to 73 percent after ICH [13,30-32]. Furthermore, ICH related to oral anticoagulant therapy is associated with a worse outcome than spontaneous ICH, as illustrated by the following reports:

The evidence regarding preceding antiplatelet use with prognosis after ICH is not as clear, with some [13,33-35] but not all [31,36-40] studies reporting worse prognosis or greater hematoma enlargement with ICH. As examples:

Reversal of anticoagulation — For patients who develop an ICH, all anticoagulant and antiplatelet drugs should be discontinued acutely for at least one to two weeks after the onset of hemorrhage, and anticoagulant effect should be reversed immediately with appropriate agents [12,63].Aggressive use of intravenous vitamin K, unactivatedprothrombin complex concentrate (also called factor IX complex), and other factors may be necessary in patients who suffer an ICH while taking warfarin. Reversal of anticoagulation in this setting is discussed in detail separately. (See &quot;Management of warfarin-associated intracerebral hemorrhage&quot;, section on &apos;Reversing the coagulation defect&apos;.)There is a risk of creating a prothrombotic state when acutely reversing anticoagulation in a patient with atrial fibrillation; however, the risk of extending the hemorrhage outweighs this potential risk [64].Protamine sulfate is recommended for urgent treatment of patients with heparin-associated ICH [12,63]. Protamine sulfate can be administered by slow intravenous infusion (not greater than 20 mg/min and no more than 50 mg over any 10-minute period).

Although there are few controlled trials available for guidance, the following additional management issues need to be addressed:

Thirty-day mortality rates increased steadily with ICH score; mortality rates for ICH scores of 1, 2, 3, 4, and 5 were 13, 26, 72, 97, and 100 percent, respectively. No patient with an ICH score of 0 died, and none had a score of 6 in the cohort.The ICH score has been validated by retrospective [43] and prospective [44,45] analysis. A modified ICH score [43] using the National Institutes of Health Stroke Scale (NIHSS) score [46] (table 3) in place of the GCS score may be a better predictor of good outcome than the original ICH score

Limiting care — Prognostication for individual patients with acute ICH remains an uncertain at best. Accumulating data suggest that the early use of do not resuscitate (DNR) orders, along with decisions to limit aggressive treatments and/or withdraw medical care may negatively influence outcome in patients with ICH, and may even invalidate some prognostic models that do not control for this variable [47-51].Early DNR orders or limitations to care are not always inappropriate after ICH; the difficulty lies in deciding when such limitations are indeed the most appropriate approach [48].Current guidelines suggest careful consideration of aggressive full care during the first 24 hours after ICH onset and postponement of new DNR orders during that time [12,52]. The recommendation does not apply to patients with preexisting DNR orders.

Other factors — Patient age and overall medical health and condition have an important role in the patient’s survival and morbidity after ICH.A number of reports have noted that elevated admission blood glucose after ICH is a poor prognostic indicator [4,9,53-55]. However, it is unclear if elevated glucose directly contributes to poor outcome, or if it alternatively is present secondarily as part of the stress response to severe ICH.Low total and LDL cholesterol have been linked to a risk of ICH. (See &quot;Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis&quot;, section on &apos;Risk factors&apos;.) In one study of 108 patients with ICH, lower serum LDL-cholesterol predicted early hematoma growth, neurologic deterioration, and three-month mortality [56].One study found that patients with more extensive white matter lesions assessed on admission CT scan had a higher rate of mortality [57]. Another study found that elevated C-reactive protein levels were an independent predictor of mortality after ICH [58].

Hyperglycemia — Hyperglycemia, generally defined as a blood glucose level &gt;126 mg/dL (&gt;7.0 mmol/L), is common in patients with acute ischemic stroke and is associated with poor functional outcome [17-21]. In a series of 59 patients with acute ischemic stroke, admission hyperglycemia was present in 32 percent of patients without diabetes and 81 percent of patients with diabetes [22]. Stress hyperglycemia may be the most common cause [20], although newly diagnosed diabetes is also important [21].Hyperglycemia may augment brain injury by several mechanisms including increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood brain barrier permeability. Several lines of evidence point to the deleterious effects of elevated glucose in acute stroke [23]:Hyperglycemia worsens ischemic damage in animal models of strokeGlucose reduction reduces ischemic damage in experimental modelsAcute hyperglycemia is associated with reduced salvage of penumbral tissue and greater final infarct size by neuroimaging [24]Hyperglycemia is associated with reduced benefit from recanalization with thrombolytic therapy and higher odds for symptomatic intracerebral hemorrhage [25]One underpowered clinical trial found no beneficial effect of insulin treatment for hyperglycemia in acute stroke [26]. However, in light of the evidence cited above, it is reasonable to treat severe hyperglycemia in the setting of acute stroke. The American Heart Association/American Stroke Association guidelines recommend treatment with insulin for patients who have serum glucose concentrations &gt;140 to 185 mg/dL (&gt;7.8 to 10.3 mmol/L) [1,2]. The European Stroke Initiative guidelines recommend treatment for glucose &gt;180 mg/dL (&gt;10 mmol/L) [27]. A planned NINDS-funded multicenter randomized trial (SHINE) will evaluate whether tight control of glucose with intravenous insulin improves outcome in acute ischemic stroke patients [28].

Fever is associated with unfavorable outcomes in human studies of stroke [30-34], as illustrated by the following reports:A meta-analysis analyzed fever and outcome in patients with neurologic injury, including hemorrhagic and/or ischemic stroke [30]. Fever was significantly associated with increased mortality rates, greater disability, more dependence, worse functional outcome, greater severity, and longer intensive care unit and hospital stays. These results were consistent for overall pooled data and for subgroups limited to studies of patients with hemorrhagic, ischemic, or all stroke types.A prospective study of 390 patients admitted to the hospital within six hours of stroke onset found that mortality and outcome were worse in patients with fever and better in those with mild hypothermia on admission [32]. Body temperature was independently related to the initial stroke severity and infarct size; for each 1ºC increase in body temperature, the relative risk of a poor outcome rose by 2.2.Treatment — The source of fever should be investigated and treated, and antipyretics should be used to lower temperature in febrile patients with acute stroke [1,2]. We suggest maintaining normothermia for at least the first several days after an acute stroke [29]. However, the clinical utility of this approach has not been established.The PAIS trial evaluated 1400 adults no later than 12 hours after symptom onset of acute ischemic stroke intracerebral hemorrhage [35]. Included patients had a body temperature of 36ºC to 39ºC. Compared with placebo, paracetamol (acetaminophen) 1 g six times daily for three days did not improve outcome [35]. However, a post-hoc subgroup analysis of 661 patients with a baseline body temperature of 37ºC to 39ºC suggested benefit for paracetamol.In a systematic review and meta-analysis of five small randomized controlled trials with a total of 293 patients, there was no benefit for pharmacologic temperature reduction for acute stroke [36]. All the trials enrolled patients within 24 hours of stroke onset, and the duration of treatment ranged from 24 hours to five days. With addition of results from the PAIS trial, the updated meta-analysis found no difference between active treatment and control for a favorable outcome (odds ratio 1.1, 95% CI 0.9-1.3) [35].Larger trials are needed to determine if pharmacologic temperature reduction improves outcome from acute stroke, particularly for patients with temperature of ≥37ºC, though it seems unlikely that acetaminophen will be effective by itself.Induced hypothermia is not currently recommended for patients with ischemic stroke [1], outside of clinical trials. An NINDS-funded randomized trial (ICTuS2/3) evaluating the combination of hypothermia and thrombolysis versus thrombolysis alone is currently underway [37].

Intracranial pressure control — Increased intracranial pressure (ICP) due to ICH can result from the hematoma itself and from surrounding edema, and may contribute to brain injury and neurologic deterioration. Current guidelines recommend a balanced and graded approach to the management of elevated ICP, beginning with simple measures that include the following [12]:Elevate the head of the bed to 30 degrees, once hypovolemia is excluded.Analgesia and sedation, particularly in unstable, intubated patientsSedation should be titrated to control pain and minimize ICP elevation, while still permitting clinical evaluation of the patient&apos;s neurologic status [12]. Suggested intravenous agents for sedation are propofol, etomidate, or midazolam. Suggested agents for analgesia and antitussive effect are morphine or alfentanil. Glucocorticoids should not generally be used to lower the ICP in patients with ICH. A randomized trial found that dexamethasone did not improve outcome but did increase complication rates, primarily infection [65].

CPP equals mean arterial pressure (MAP) minus ICP. Lowering ICP helps to maintain CPP in an adequate range.Monitoring and treatment of ICP should be considered for patients with GCS &lt;8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus [52]. More aggressive therapies for reducing elevated ICP include osmotic diuretics (eg, mannitol and hypertonic saline solution), ventricular catheter drainage of cerebrospinal fluid, and neuromuscular blockade with the goal of maintaining cerebral perfusion pressure (CPP) of 50 to 70 mmHg [12,52]. However, the development of cerebral ischemia is still possible even with CPP-guided therapy.

Barbiturate anesthesia can be used if mannitol fails to lower ICP to an acceptable range. Barbiturate coma acts by reducing cerebral metabolism, which results in a lowering of cerebral blood flow and thus decreases ICP [12]. It is of variable benefit for the treatment of elevated ICP from a variety of causes and is associated with a high rate of severe side effects, especially arterial hypotension [68]. Continuous electroencephalogram monitoring is suggested during high-dose barbiturate treatment, with the dose titrated to a burst-suppression pattern of electrical activity [12].The ICP lowering effect of hyperventilation to a PaCO2 of 25 to 30 mmHg is dramatic and rapid. However, the effect only lasts for minutes to a few hours. Thus, we reserve hyperventilation until the above therapies have been maximized [69].

Blood pressure control — The mean arterial pressure (MAP) is often elevated in patients with ICH. Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding [75]. However, an increased MAP may be necessary to maintain cerebral perfusion in some patients, and lowering the arterial pressure (eg, to a systolic blood pressure [SBP] below 130 mmHg) may cause ischemia and worsen neurologic injury.Limited prospective data are available regarding blood pressure management in ICH. In a randomized controlled trial (INTERACT) of 404 patients with acute spontaneous ICH, intensive blood pressure lowering treatment (target systolic blood pressure 140 mmHg) compared with traditional management (target systolic blood pressure 180 mmHg) was associated with a reduction in hematoma growth at 24 hours (14 versus 26 percent) [76,77]. However, this finding did not achieve statistical significance after adjustment for initial hematoma volume and time from ICH onset to head CT. There was no effect of treatment on clinical outcomes at 90 days. A larger trial (INTERACT2) is in progress. Smaller, nonrandomized studies have also found that more aggressive blood pressure lowering is associated with strong trends toward reduced hematoma enlargement [12,77-79]. In some studies, there were also trends toward reduced perilesional edema and better clinical outcomes.

Seizure prophylaxis and treatment — The risk of seizures in patients with acute spontaneous ICH ranges from 4.2 to 29 percent [12]. Seizures are more common in lobar as compared to deep hemorrhage [80]. The frequency depends in part on the extent of monitoring, as seizures associated with ICH are often nonconvulsive [12]. (See &quot;Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis&quot;, section on &apos;Clinical presentation&apos;.)If a seizure occurs, appropriate intravenous antiepileptic drug (AED) treatment should be administered to prevent recurrent seizures [52]. The choice of the initial antiepileptic agent depends upon individual circumstances and contraindications. Current guidelines suggest the use of intravenous fosphenytoin or phenytoin in this setting [12].While some experts suggest a brief period of AED prophylaxis soon after ICH onset as a potential means of reducing the risk for early seizures in patients with lobar hemorrhages [12], 2010 guidelines recommend against prophylactic use of AEDs [52]

Resumption of antiplatelet therapy — A common question is when patients can resume antiplatelet therapy after suffering an ICH. Our experience with the use of aspirin suggests that it is probably safe to resume therapy after the acute phase of ICH provided that blood pressure is well controlled and that the indication for antiplatelet treatment is sufficiently strong that the potential benefit outweighs the increase in risk of recurrent ICH.Unfortunately, there are limited data that specifically address this issue. Therefore, most decisions must be made by extrapolating from the limited data regarding antiplatelet therapy and the risk of primary ICH. The best available data comes from meta-analyses of randomized controlled trials; these suggest that aspirin use is associated with an approximately 40 percent relative increase in the risk of initial ICH, which translates into a very small absolute increase in risk [103,104].(See &quot;Anticoagulant and antiplatelet therapy in patients with an acute or prior intracerebral hemorrhage&quot;, section on &apos;Aspirin and warfarin therapy&apos;.) In the setting of cerebral amyloid angiopathy, aspirin use may be associated with a greater risk of recurrent ICH [105]. (See &quot;Cerebral amyloid angiopathy&quot;, section on &apos;Avoidance of anticoagulants and antiplatelet agents&apos;.)Although aspirin reduces the risk of ischemic stroke by 25 percent, this benefit is largely negated by the associated increased risk of recurrent ICH, which typically causes more disability than ischemic stroke. Therefore, we do not recommend aspirin or antiplatelets for those patients with only an &quot;average&quot; risk of recurrent ischemic stroke. What exactly constitutes &quot;average&quot; or &quot;above average&quot; risk is not certain, but we consider hypertension, diabetes, hypercholesterolemia, and the absence of heart disease to be markers of average risk. Atrial fibrillation, cardiomyopathy, large vessel extracranial and intracranial stenoses, and malignancy can be considered as markers for those with &quot;above average&quot; risk who may benefit from long-term antiplatelet therapy after ICH.We do not recommend resumption of aspirin or antiplatelets for primary prevention of cardiovascular disease. In the few existing primary prevention studies, patients with any prior ICH were excluded. Such patients should avoid aspirin unless a compelling indication for aspirin use develops later on.

Timing and dose — The timing of antiplatelet use after ICH is largely empiric. There is risk of rebleeding and hematoma expansion in the first several hours. At 10 days, rebleeding is unlikely. The AHA/ASA guidelines of 2006 state that antiplatelets should be discontinued for at least one to two weeks [106].Some experts have argued that aspirin can be used safely as soon as 48 hours after ICH in those who require prophylaxis for venous thromboembolism. We agree, provided neuroimaging has demonstrated a stable ICH. If aspirin is used after ICH, we agree with others that a lower dose (30 to 160 mg daily) is both effective and safer than higher doses.

3.
MORTALITY AND FUNCTIONAL OUTCOME
• Furthermore, only a small number of patients function
independently after the event.
• In a prospective study of 166 patients with spontaneous ICH
from a large US metropolitan area, only 12 percent were normal
or minimally handicapped at 30 days [1].
• A systematic review estimated that between 12 and 39 percent
of patients achieve independent function [2].
1.
Daverat P, Castel JP, Dartigues JF, Orgogozo JM. Death and functional outcome after spontaneous intracerebral
hemorrhage. A prospective study of 166 cases using multivariate analysis. Stroke 1991; 22:1.
2.
van Asch CJ, Luitse MJ, Rinkel GJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage
over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol 2010; 9:167.

4.
MODIFIED RANKIN SCALE
Score
Description
0
No symptoms at all
1
No significant disability despite symptoms; able to carry out
all usual duties and activities
2
Slight disability; unable to carry out all previous activities,
but able to look after own affairs without assistance
3
Moderate disability; requiring some help, but able to walk
without assistance
4
Moderately severe disability; unable to walk without
assistance and unable to attend to own bodily needs
without assistance
5
Severe disability; bedridden, incontinent and requiring
constant nursing care and attention
6
Dead

9.
INITIAL ICH VOLUME AND LEVEL OF
CONSCIOUSNESS
In a study of 188 patients with ICH that analyzed predictors of 30day mortality [1]; the following observations were made:
• An ICH vol of ≥60 cm3 on initial CT and a GCS score of ≤8
predicted a 30-day mortality of 91 %.
• An ICH vol <30 cm3 and a GCS score of ≥9 predicted a 30-day
mortality of 19 %..
1. Fogelholm R, Murros K, Rissanen A, Avikainen S. Long term survival after primary intracerebral
haemorrhage: a retrospective population based study. J Neurol Neurosurg Psychiatry 2005; 76:1534.

10.
HEMATOMA GROWTH
• In a meta-analysis of 218 patients with spontaneous ICH who
had a head CT scan within three hours of onset and follow-up
head CT within 24 hours, each 10 % increase in ICH growth was
associated with increased mortality (hazard ratio 1.05, 95% CI
1.03-1.08) and worse outcome as measured by the modified
Rankin scale (odds ratio 0.84, 95% CI 0.75-0.92) [1].
• That is, for each 10 % increase in hematoma volume, patients
were 5 percent more likely to die and 16 % more likely to
increase one point on the modified Rankin scale..
1.
Davis SM, Broderick J, Hennerici M, et al. Hematoma growth is a determinant of mortality and poor outcome after
intracerebral hemorrhage. Neurology 2006; 66:1175.

11.
INTRAVENTRICULAR EXTENSION
• One of the largest of these reports evaluated 406 patients with
ICH, 45 % of whom had intraventricular extension of
hemorrhage. [1].
• After controlling for age and ICH volume, a poor outcome at
discharge (defined as a modified Rankin scale score of 4 to 6)
was significantly more likely in patients with intraventricular
hemorrhage than in those without intraventricular hemorrhage
(odds ratio 2.25, 95% CI 1.40-3.64)..
1.
Hallevi H, Albright KC, Aronowski J, et al. Intraventricular hemorrhage: Anatomic relationships and clinical
implications. Neurology 2008; 70:848.

12.
EARLY NEUROLOGIC DETERIORATION
• In a prospective study of 266 patients with ICH admitted within 12 hrs of
stroke onset, early neurologic deterioration occurred in 61 (23%) and was
associated with an 8-fold ↑ in the probability of a poor outcome (95% CI
2.7-25.5) [1].
• Independent predictors of early neurologic deterioration on admission
included elevations in body temperature, neutrophil count, and serum
fibrinogen level (odds ratios 24.5, 2.1, and 5.6, respectively), all of which
could be interpreted as markers of an inflammatory response.
• Factors measured at 48 hours that were associated with early neurologic
deterioration included ICH growth on repeat head CT, intra ventricular
bleeding, and high systolic BP.
1.
Leira R, Dávalos A, Silva Y, et al. Early neurologic deterioration in intracerebral hemorrhage: predictors and
associated factors. Neurology 2004; 63:461.

16.
REVERSAL OF ANTICOAGULATION
RECOMMENDATION
• For patients who develop an ICH, all anticoagulant and antiplatelet drugs
should be discontinued acutely for at least one to two weeks after the onset
of hemorrhage, [1,2].
• Aggressive use of intravenous vitamin K and other factors may be necessary
in patients who suffer an ICH while taking warfarin. (class I. Level of Evidence: B)
• There is a risk of creating a prothrombotic state when acutely reversing
anticoagulation in a patient with atrial fibrillation; however, the risk of
extending the hemorrhage outweighs this potential risk [3].
• Protamine sulfate is recommended for urgent treatment of patients with
heparin-associated ICH [1,2]. (class I. Level of Evidence: B)
1.
Broderick J, Connolly S, et al. Guidelines for the management of spontaneous intracerebral hemorrhage .A guideline for Healthcare Professionals
from the American Heart Association/American Stroke Association. Stroke 2010
2.
Furie KL, Kasner SE, Adams RJ, et al. Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for
healthcare professionals from the american heart association/american stroke association. Stroke 2011; 42:227.
3.
Genewein U, Haeberli A, Straub PW, Beer JH. Rebound after cessation of oral anticoagulant therapy: the biochemical evidence. Br J Haematol 1996;
92:479.

18.
ADDITIONAL MANAGEMENT ISSUES
• Keeping the systolic blood pressure <180 mmHg during the acute phase is
advisable.
• Given the high mortality accompanying AAICH, surgical evacuation of the
hematoma after reversing anticoagulation can be considered in selected
patients.
• For patients who will resume anticoagulation, Warfarin can be restarted at 7
to 10 days. (class IIb. Level of Evidence: B)
• Pneumatic compression stockings and early ambulation should be
considered if leg paresis is present. (class I. Level of Evidence: B)

25.
OTHER FACTORS: CHOLESTEROL /STATIN
• One case-control study found that statin use prior to ICH was
associated with reduced mortality (OR 0.47) and increased
probability of a favorable outcome (OR = 2.08) with similar
results found in a meta-analysis of published studies of ICH and
statin use (n:936 vs 2284) [1].
1.
Biffi A, Devan WJ, Anderson CD, et al. Statin use and outcome after intracerebral hemorrhage: case-control study and metaanalysis. Neurology 2011; 76:1581.

28.
FEVER
•
The PAIS trial evaluated 1400 adults no later than 12 hours after symptom onset of acute
ischemic stroke and intracerebral hemorrhage [1]. Included patients had a body
temperature of 36ºC to 39ºC. Compared with placebo, paracetamol (acetaminophen) 1 g
six times daily for three days did not improve outcome [1].
•
In a systematic review and meta-analysis of five small randomized controlled trials with a
total of 293 patients, there was no benefit for pharmacologic temperature reduction for
acute stroke [2]. All the trials enrolled patients within 24 hours of stroke onset, and the
duration of treatment ranged from 24 hours to five days. With addition of results from the
PAIS trial, the updated meta-analysis found no difference between active treatment and
control for a favorable outcome (odds ratio 1.1, 95% CI 0.9-1.3) [1].
1.
den Hertog HM, van der Worp HB, van Gemert HM, et al. The Paracetamol (Acetaminophen) In Stroke (PAIS) trial: a
multicentre, randomised, placebo-controlled, phase III trial. Lancet Neurol 2009; 8:434.
2.
Den Hertog HM, van der Worp HB, Tseng MC, Dippel DW. Cooling therapy for acute stroke. Cochrane Database Syst Rev
2009; :CD001247
.

29.
RECOMMENDATION ON FEVER
• The source of fever should be investigated and treated, and
antipyretics should be used to lower temperature in febrile patients
with acute stroke [1,2].
• It is suggested maintain normothermia for at least the first several
days after an acute stroke [3].
• Induced hypothermia is not currently recommended for patients
with ischemic stroke [1], outside of clinical trials.
1.
Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the
American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and
Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary
Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke
2007; 38:1655.
2.
Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007
update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research
Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007; 38:2001.
3.
Ginsberg MD, Busto R. Combating hyperthermia in acute stroke: a significant clinical concern. Stroke 1998; 29:529.

32.
INTRACRANIAL PRESSURE CONTROL
• Elevate the head of the bed to 30 degrees, once hypovolemia is
excluded.
• Analgesia and sedation, particularly in unstable, intubated patients
• Suggested intravenous agents for sedation are propofol, or
midazolam.
• Suggested agents for analgesia and antitussive effect are morphine or
alfentanil.
• Glucocorticoids should not generally be used to lower the ICP in
patients with ICH. A randomized trial found that dexamethasone did
not improve outcome but did increase complication rates, primarily
infection [1].
1.
Poungvarin N, Bhoopat W, Viriyavejakul A, et al. Effects of dexamethasone in primary supratentorial intracerebral hemorrhage. N Engl J Med
1987; 316:1229.

33.
MANAGING ICP
• Monitoring and treatment of ICP should be considered for
patients with GCS <8, those with clinical evidence of
transtentorial herniation, or those with significant IVH or
hydrocephalus [1].
1.
Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral
hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke 2010; 41:2108.

34.
LOWERING ICP
•
Intravenous mannitol is the treatment of choice to lower increased intracranial
pressure, effectively lowering ICP and benefiting brain metabolism [1].
•
It is administered as an initial bolus of 1 g/kg, followed by infusions of 0.25 to
0.5 g/kg every six hours.
•
The goal of therapy is to achieve plasma hyperosmolality (300 to 310
mosmol/kg) while maintaining an adequate plasma volume; major side effects
include hypovolemia and a hyperosmotic state [2].
•
Normal saline initially should be used for maintenance and replacement fluids;
hypotonic fluids are contraindicated.
•
Dextrose-containing fluids should be avoided unless hypoglycemia is present or strongly suspected because
excessive glucose may be injurious to stroke patients. [2].
1.
Helbok R, Kurtz P, Schmidt JM, et al. Effect of mannitol on brain metabolism and tissue oxygenation in severe haemorrhagic stroke. J Neurol
Neurosurg Psychiatry 2011; 82:378.
2.
Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a
guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the
Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007; 38:2001.

39.
SEIZURE PROPHYLAXIS AND TREATMENT
•
The risk of seizures in patients with acute spontaneous ICH ranges from 4.2 to 29 percent [1].
Seizures are more common in lobar as compared to deep hemorrhage [3].
•
If a seizure occurs, appropriate iv AED treatment should be administered to prevent recurrent
seizures [2].
•
The choice of the initial antiepileptic agent depends upon individual circumstances and
contraindications.
•
Current guidelines suggest the use of intravenous fosphenytoin or phenytoin in this setting [1].
•
While some experts suggest a brief period of AED prophylaxis soon after ICH onset as a
potential means of reducing the risk for early seizures in patients with lobar hemorrhages [1],
2010 guidelines recommend against prophylactic use of AEDs [2]
1.
Broderick J, Connolly S, Feldmann E, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007
update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure
Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Stroke 2007; 38:2001.
2.
Morgenstern LB, Hemphill JC 3rd, Anderson C, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a
guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2010; 41:2108.
3.
Kuramatsu JB, Sauer R, Mauer C, et al. Correlation of age and haematoma volume in patients with spontaneous lobar intracerebral
haemorrhage. J Neurol Neurosurg Psychiatry 2011; 82:144.

42.
SURGERY
• For patients with cerebellar hemorrhages >3 cm in diameter who
are deteriorating or who have brainstem compression and/or
hydrocephalus due to ventricular obstruction, it is recommended
for surgical removal of hemorrhage.
• Surgery for supratentorial ICH is controversial, and current
guidelines suggest consideration of standard craniotomy only
for those who have lobar clots within 1 cm of the surface.
• The routine evacuation of supratentorial ICH in the first 96 hours
is not recommended.

43.
INTRAVENTRICULAR HEMORRHAGE
• Patients with intraventricular extension of the ICH are at risk for
hydrocephalus, especially if the third and fourth ventricles are
involved.
• Such patients should be closely monitored.
• When neurologic deterioration occurs, an emergent CT scan
should be done to exclude the development of hydrocephalus.
• Patients with neurologic deterioration in the setting of ventricular
enlargement may be candidates for ventriculostomy and
external ventricular drainage.

44.
RESUMPTION OF ANTIPLATELET THERAPY
•
It is probably safe to resume therapy after the acute phase of ICH provided that
blood pressure is well controlled and that the indication for antiplatelet treatment
is sufficiently strong that the potential benefit outweighs the increase in risk of
recurrent ICH.
•
The best available data comes from meta-analyses of randomized controlled
trials; these suggest that aspirin use is associated with an approximately 40
percent relative increase in the risk of initial ICH, which translates into a very
small absolute increase in risk [1,2).
•
In the setting of cerebral amyloid angiopathy, aspirin use may be associated with
a greater risk of recurrent ICH [3].
1.
He J, Whelton PK, Vu B, Klag MJ. Aspirin and risk of hemorrhagic stroke: a meta-analysis of randomized controlled trials. JAMA 1998; 280:1930.
2.
Hart RG, Halperin JL, McBride R, et al. Aspirin for the primary prevention of stroke and other major vascular events: meta-analysis and hypotheses.
Arch Neurol 2000; 57:326.
3.
Biffi A, Halpin A, Towfighi A, et al. Aspirin and recurrent intracerebral hemorrhage in cerebral amyloid angiopathy. Neurology 2010; 75:693.

45.
• Although aspirin reduces the risk of ischemic stroke by 25 percent, this
benefit is largely negated by the associated increased risk of recurrent ICH,
which typically causes more disability than ischemic stroke.
• Therefore, it is not recommended aspirin or anti-platelets for those patients
with only an "average" risk of recurrent ischemic stroke.
• “Average" risk : HTN, DM, hypercholesterolemia, and the absence of heart
disease .
• “Above Average" risk : Atrial fibrillation, cardiomyopathy, large vessel
extracranial and intracranial stenoses, and malignancy :may benefit from
long-term antiplatelet therapy after ICH.

46.
TIMING AND DOSE
• The timing of antiplatelet use after ICH is largely empiric. There
is risk of rebleeding and hematoma expansion in the first
several hours. At 10 days, rebleeding is unlikely.
• The AHA/ASA guidelines of 2006 state that antiplatelets should
be discontinued for at least one to two weeks [1].
• If aspirin is used after ICH, a lower dose (30 to 160 mg daily) is
both effective and safer than higher doses.
1.
Sacco RL, Adams R, Albers G, et al. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack:
a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: cosponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of
this guideline. Stroke 2006; 37:577.